The left panel shows treated and untreated cells in regards to the common cold virus (rhinovirus) while the right panel shows treated and untreated monkey cells in regards to dengue hemorrhagic fever virus (Source: Massachusetts Institute of Technology)

Double-stranded RNA Activated Caspase Oligomerizers (DRACOs) could be the answer for terminating viruses like H1N1 influenza, stomach viruses, a polio virus, several types of hemorrhagic fever and dengue fever

Viruses like the common cold and influenza are infections that we occasionally must ride out. All anyone can really do is rest and take medications to ease the symptoms, which can range from congestion to fever to vomiting. Other viruses, such as Ebola, can be potentially fatal due to Ebola hemorrhagic fever.

While many bacterial infections can be treated with antibiotics, not many viral infections can be treated with medications. Only a "handful" can fight viruses, like the protease inhibitors to control HIV, but most other treatments only relieve the symptoms, and even that can take several days in some cases. Viruses are difficult to attack because they change and replicate in healthy cells.

But now, a team of researchers at MIT's Lincoln Laboratory may have found the cure for the common cold as well as many other viruses like H1N1 influenza, stomach viruses, a polio virus, several types of hemorrhagic fever and dengue fever. The team, led by Todd Rider, a senior staff scientist in Lincoln Laboratory's Chemical, Biological and Nanoscale Technologies Group, created therapeutic agents called Double-stranded RNA Activated Caspase Oligomerizers (DRACOs) which have successfully terminated viral infections.

Viruses infect cells by taking over the cell entirely and multiplying. While making copies of themselves, the viruses also produce long strings of double-stranded RNA (dsRNA). This is not found in animal or human cells.

To fight these infected cells, healthy human cells have proteins that bind to dsRNA, which then prompts a series of reactions that work to stop the virus from making copies of itself. The problem is that the virus can block one of the healthy cells' series of steps to prevent its replication somewhere down the line, allowing the virus to change and further reproduce once again.

To remedy this problem, Rider and his team mixed a dsRNA protein with another protein that causes cells to go through apoptosis, which is programmed cell suicide. One end of the DRACO binds to dsRNA while the other end is instructed to launch cell suicide.

Also, each DRACO consists of a "delivery tag" that they received from naturally occurring proteins. This allows it to enter any human or animal by crossing cell membranes, meaning that it can combat a broad spectrum of viruses, possibly including new outbreaks.

The team tested the DRACOs in human and animal cells cultured in the lab as well as mice infected with the H1N1 influenza virus. They found that DRACO left the mice fully cured of the infection, and that DRACO is not toxic to these animals. In addition, DRACO only targeted cells with dsRNA present while leaving healthy cells alone.

Rider and his team are now testing DRACO on other viruses in mice, and hope to eventually test it on larger animals and humans.

When I hear about this sort of stuff, it makes me incredibly uneasy. It goes without saying that micro-organisms replicate and evolve unbelievably fast. Whatever "weapon" they think they've found, the viruses WILL adapt, they WILL become resistant, and in the end they'll emerge stronger than they ever were before.

Just look at bacteria and antibiotics. Super-resistant strains of diseases we thought were no longer a problem.....people dying from simple staph infections. The skat hasn't even completely hit the fan yet in that regard.

The ONLY way to attack a disease is to completely wipe it off the map; like we did with smallpox and polio. Other than that......rest and keep a healthy immune system.

Bacteria and their antibiotic resistance has been evolving rapidly in the last couple decades, but much of that is our own fault.

Doctors prescribing antibiotics unnecessarily, and patients not completing the whole treatment or using antibiotics for things it has no use (like, taking antibiotics because they've caught a cold).

As an example, tuberculosis is becoming a bigger problem in many places. Something that was simpler in the past now has strands that are virtually incurable. There is a number of patients that stop taking their antibiotics as soon as their symptoms disappear, instead of completing the whole treatment cycle. The disease returns, and this time resistant to those drugs. Depending on what antibiotics they were using to begin with, it could now be fatal.

You must have a bad doctor. I've heard it from every single doctor. I rarely go to the doctor, but my daughter and ex-wife did. Each time I was with them they were adamant about completing the entire round of antibiotics.

He probably has an HMO plan they barely look at you all they do is give you a prescription and if your alive in a few days they may look at you again. Its close to a witch doctor with the ability to prescribe medication.

First, this isn't a single treatment, it's a potential new class of treatments if demonstrated to be safe in humans.

Similar to how the discovery of penicillin sparked the antibiotic revolution. There has been tremendous advancement and penicillin is nothing like modern antibiotics, the ONLY similarity is that they attack peptidoglycan in bacterial cell walls.

Second, the ability to bind to dsRNA is the real advancement here. While viruses will probably adapt by modifying targeted binding sites, if the technique works, we can simply modify the binding end of the molecule to either another binding site or the adapted binding site.

Third, to wipe a disease off the map, you have 1 of two approaches. The first is to vaccinate the entire population against a virus quickly enough, that the natural reservoirs die out before a virus adapts. IE, smallpox and polio. Both are extinct not because we killed them all, but because there is not longer a large population vulnerable to them for them to gain a foothold.

I can kill viruses or bacteria a hundred different ways in the lab. Killing bacteria or viruses with 100% effectiveness is very easy. The hard part is finding a way that doesn't kill the host at the same time. The solution is to target a factor unique to the pathogen and target it. Despite your hyperbole, antibiotics have saved millions of lives since their inception and they work because they target a compound unique to bacteria, peptidoglycan, so no matter how strongly we target it, we won't directly harm any human cells.

Antibiotics are far from ineffective, and we've "wiped off the map" many infectious strains of bacteria. The classic example would be the strains of yersinis pestis responsible for the "black death" plagues in Europe.

Up till now, it has been very difficult to target something unique to viruses, this is one promising approach.

The worldwide mortality rate dropped tremendously after the invention of antibiotics. Infant mortality dropped 52% in the years after the discovery of penicillin and despite your alarmist views, it has only decreased since then. Infant mortality the probably the best indicator of a populations vulnerability to pathogens as they are one of the weakest populations against them.

If this new approach results in an antibiotic like approach for treating ds viral diseases, it nothing but good news for humanity.

I absolutely agree with banthracis on 99% of his points. Penicillin was the first beta lactam antibiotic we discovered, and from our knowledge of its activity we were able to generate several distinct antibiotics without even modifying the beta lactam ring structure. From there, we created new classes of antibiotics that don't use beta lactam rings to inhibit peptidoglycan formation and instead attack other unique aspects of bacterial physiology, such as bacterial ribosomes.

Antibiotics and vaccination, alongside improved sanitary conditions, were responsible for the jump in average life expectancy from a high of around 50 at the turn of the 20th century to an average of around 75 years at the turn of the 21st. While having an effective tool against viral infections will be useful for combating infectious disease, the current limitation to human life expectancy is the prevalence of cancers associated with aging, breakdown of vasculature associated with aging, and neurodegeneration associated with aging. If we can overcome these challenges who knows what length and quality of life humans might be able to achieve.

We won't need to modify dsRNA binding protein. Any dsRNA will be bound just by the virtue of being dsRNA. Nothing in the sequence is required, so there's nothing the viruses can change. That's part of the beauty of this: the virus isn't what's being targeted, it's our own cellular pathways that are ubiquitous yet unique solely to the viral infected state.

What part am I wrong about? The fact that the viruses will evolve and eventually find a way to become resistant to the treatment? You'd have to be pretty naive to think that they won't.

No matter what you do, there will always be doctors who over-prescribe and people who don't take the medication properly. In the short term, these treatments will probably be incredibly effective and save many lives. Some strains may be wiped out altogether, but not all of them will. In the long term, we will need to constantly alter the way the treatments work in order for them to remain effective, and we will also end up with a handful of super-resistant viruses that can get really out of hand.

Of course, that last result might be something that takes 50+ years to happen. I still think we're some years off from seeing the ramifications of our antibacterial/antibiotic use that started in the 1930's.

And what would they evolve and change? Do you know how this is working? It isn't going after the virus, it's going after viral infected parts of you.

Or, do you know how bacteria gain resistance to antibiotics? Antibiotics attack some part of the bacteria, and they either start overexpressing a protein that digests the antibiotic (common), pump it out of their cells, or modify the antibiotic's target (very rare) so it's no longer applicable. A virus has no control over how your cells are designed to work; they can only co-op the machinery that's already there to do their bidding. Think about how resistance actually works, for a minute; also realize it's not an all or nothing thing, it's simply changing the sliding scale of dosage higher and higher. Our medicine is also staying head of the resistance game, and bacteria don't simply gain a resistance and keep it forever--it's a constant tug of war. There will always be working antibiotics.

Bacteria and viruses are quite different in how they mutate and share genes as well. Bacteria are promiscuous, and can give each other a solution to a problem. Viruses don't, they can only pull out host factors (very rare) or modify what they already have using low fidelity replication (common, made into an art form by HIV). Since, again, this treatment does not bother with any actual part of the viruses themselves, there is nothing of their own proteins they can modify to have any effect.

There are still theoretically ways they could garner resistance, but they would be highly specific, easily circumvented, and very hard to gain. The greatest challenge would be your own immune system identifying the treatment protein and destroying it before it has a chance to act. That is the greatest barrier, and a type of resistance you could gain on the fly.

Egglick...you should chop your head off now and unburden the human race of your alarmist stupidity.

That being said...viruses are also not nearly as adaptable as bacteria. There is a lot less to work with.

Yes, every time antibiotics are taken for the wrong reason it increases the chances of a resistant mutation. Additionally, every time antibiotics are taken for the right reason it increases the chances of a resistant mutation. If antibiotics are used at all, for any reason, the chances of a resistant mutation are increased. Because, if the antibiotic kills a million bacteria...it leaves 20 or so bacteria that happen to have a mutation that resists the antibiotic...if these resistant bacteria thrive...you may have a superbug. But it doesnt matter as science marches on...we will eventually get those bugs too. It really comes down to science v. mutation...and I put my money on science.

And, on a related note...this is possibly a HUGE breakthrough...right up there with the Kanzius Machine. I really hope this DRACO makes it through human trials.

Apoptosis is apopotosis man. Re-read about how the mechanisms work here. We are binding the virus to the cell and then cause the cell to kill itself--i.e. suicide. The virus dies with the cell. It doesn't get the opportunity to evolve here.

That's also the scary thing--to know that inside you your cells are dying off as a result of the treatment. However, a lot of times viruses either mutate or kill off the host cell anyways so it is pretty much a wash.